scholarly journals The Mediation Role of Dynamic Multisensory Processing Using Molecular Genetic Data in Dyslexia

2020 ◽  
Vol 10 (12) ◽  
pp. 993
Author(s):  
Sara Mascheretti ◽  
Valentina Riva ◽  
Bei Feng ◽  
Vittoria Trezzi ◽  
Chiara Andreola ◽  
...  
Keyword(s):  
Candidate Genes ◽  
Auditory Processing ◽  
Visual Motion ◽  
Multisensory Processing ◽  
Molecular Genetic ◽  
Rapid Automatized Naming ◽  
Motion Processing ◽  
Visual Motion Processing ◽  
Molecular Genetic Data ◽  
Rapid Auditory Processing

Although substantial heritability has been reported and candidate genes have been identified, we are far from understanding the etiopathogenetic pathways underlying developmental dyslexia (DD). Reading-related endophenotypes (EPs) have been established. Until now it was unknown whether they mediated the pathway from gene to reading (dis)ability. Thus, in a sample of 223 siblings from nuclear families with DD and 79 unrelated typical readers, we tested four EPs (i.e., rapid auditory processing, rapid automatized naming, multisensory nonspatial attention and visual motion processing) and 20 markers spanning five DD-candidate genes (i.e., DYX1C1, DCDC2, KIAA0319, ROBO1 and GRIN2B) using a multiple-predictor/multiple-mediator framework. Our results show that rapid auditory and visual motion processing are mediators in the pathway from ROBO1-rs9853895 to reading. Specifically, the T/T genotype group predicts impairments in rapid auditory and visual motion processing which, in turn, predict poorer reading skills. Our results suggest that ROBO1 is related to reading via multisensory temporal processing. These findings support the use of EPs as an effective approach to disentangling the complex pathways between candidate genes and behavior.

scholarly journals Temporal Auditory and Visual Motion Processing of Children Diagnosed with Auditory Processing Disorder and Dyslexia

2009 ◽  
Vol 30 (6) ◽  
pp. 675-686 ◽  
Author(s):  
Piers Dawes ◽  
Tony Sirimanna ◽  
Martin Burton ◽  
Iynga Vanniasegaram ◽  
Frances Tweedy ◽  
...  
Keyword(s):  
Auditory Processing ◽  
Visual Motion ◽  
Auditory Processing Disorder ◽  
Motion Processing ◽  
Visual Motion Processing

Pursuit and optokinetic deficits following chemical lesions of cortical areas MT and MST

1988 ◽  
Vol 60 (3) ◽  
pp. 940-965 ◽  
Author(s):  
M. R. Dursteler ◽  
R. H. Wurtz
Keyword(s):  
Eye Movements ◽  
Visual Field ◽  
Visual Motion ◽  
Ibotenic Acid ◽  
Motion Processing ◽  
Temporal Area ◽  
Target Speed ◽  
Pursuit Eye Movements ◽  
Medial Superior Temporal ◽  
Visual Motion Processing

1. Previous experiments have shown that punctate chemical lesions within the middle temporal area (MT) of the superior temporal sulcus (STS) produce deficits in the initiation and maintenance of pursuit eye movements (10, 34). The present experiments were designed to test the effect of such chemical lesions in an area within the STS to which MT projects, the medial superior temporal area (MST). 2. We injected ibotenic acid into localized regions of MST, and we observed two deficits in pursuit eye movements, a retinotopic deficit and a directional deficit. 3. The retinotopic deficit in pursuit initiation was characterized by the monkey's inability to match eye speed to target speed or to adjust the amplitude of the saccade made to acquire the target to compensate for target motion. This deficit was related to the initiation of pursuit to targets moving in any direction in the visual field contralateral to the side of the brain with the lesion. This deficit was similar to the deficit we found following damage to extrafoveal MT except that the affected area of the visual field frequently extended throughout the entire contralateral visual field tested. 4. The directional deficit in pursuit maintenance was characterized by a failure to match eye speed to target speed once the fovea had been brought near the moving target. This deficit occurred only when the target was moving toward the side of the lesion, regardless of whether the target began to move in the ipsilateral or contralateral visual field. There was no deficit in the amplitude of saccades made to acquire the target, or in the amplitude of the catch-up saccades made to compensate for the slowed pursuit. The directional deficit is similar to the one we described previously following chemical lesions of the foveal representation in the STS. 5. Retinotopic deficits resulted from any of our injections in MST. Directional deficits resulted from lesions limited to subregions within MST, particularly lesions that invaded the floor of the STS and the posterior bank of the STS just lateral to MT. Extensive damage to the densely myelinated area of the anterior bank or to the posterior parietal area on the dorsal lip of the anterior bank produced minimal directional deficits. 6. We conclude that damage to visual motion processing in MST underlies the retinotopic pursuit deficit just as it does in MT. MST appears to be a sequential step in visual motion processing that occurs before all of the visual motion information is transmitted to the brainstem areas related to pursuit.(ABSTRACT TRUNCATED AT 400 WORDS)

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